The Two Amino Terminal Transforming Functions of the SV40 Large T-Antigen are Required to Overcome P53 Mediated Growth Arrest

摘要: About 60% of cancers from humans contain mutations at the p53 locus1,2. Most commonly, there is a missense mutation in one alleles and loss second allele resulting reduction to homozygosity mutant gene3. Thus behaves like tumor suppressor gene4 where function (recessive wild-type) enhances probability cancerous growth. Returning wild-type gene into cells that are being transformed by an oncogene5 or already transformed6 blocks transformation process and, when expressed high levels, inhibits cell division cells. Cells with temperature sensitive replicate 37–39°C, protein conformation, but fail grow 32°C, acting as wild type suppressor1–8. The progression through cycle G1 7,8. Thus, can, under certain circumstances9, regulate while proteins do this. protein, not can act transcription factor10–12 so it tempting speculate p53-mediated set genes block phase cycle.